Host–pathogen interaction is considered a highly dynamic process between diverse microbial pathogens and hosts in all stages of pathogenic infection, from invasion to dissemination. Upon pathogenic infection, innate immune systems respond to pathogen-associated molecular patterns and activate immediate host inflammatory and antimicrobial responses 1 , 2 . Innate immune cells trigger sophisticated intracellular signaling pathways via innate immune receptors, including membrane-bound or cytosolic receptors 1 , 2 , 3 . Host innate immune activation results in the production of multiple effector molecules, including cytokines and chemokines as well as antimicrobial proteins, to combat invading pathogens and parasites 4 . In addition, innate immune cells, such as macrophages and dendritic cells, are the principal antigen-presenting cells that activate T cells, which are involved in more specific and delicate immune responses 5 , 6 . In particular, Th1 cell-mediated interferon (IFN)-γ can efficiently promote cell-autonomous host defenses against intracellular parasitic and mycobacterial infections through various effectors, including IFN-inducible GTPases, inducible nitric oxide synthase, and autophagy proteins 7 , 8 .
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Eun‐Kyeong Jo (2019) studied this question.
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